Chorangiosis is a placental vascular abnormality characterized by excessive capillarization in terminal chorionic villi, often associated with chronic placental hypoxia. It is observed in 5%–7% of placentas from neonates admitted to neonatal intensive care units and correlates with adverse maternal and fetal outcomes. We report a case of a chorangiosis of the placenta revealed in an 18-year-old primigravida who presented with moderate anemia, fetal growth restriction, oligohydramnios, and underwent elective cesarean section at 36 + 5 weeks. Chorangiosis has been linked to adverse outcomes, including stillbirth and maternal morbidity. This case highlights the importance of considering chorangiosis in the differential diagnosis of placental lesions with atypical ultrasound features. Early recognition, close fetal surveillance, and timely delivery are crucial for optimizing perinatal outcomes in such scenarios.
Chorangioma ; Hemangioma ; Fetal Growth Retardation ; Hypoxia

Preeclampsia and intrauterine growth restriction (IUGR) of the fetus are the two most common pregnancy complications worldwide, affecting 5%-10% of pregnant women. Preeclampsia is associated with significantly increased maternal and fetal morbidity and mortality. Hypoxia-induced uteroplacental dysfunction is now recognized as a key pathological factor in preeclampsia and IUGR. Reduced oxygen supply (hypoxia) disrupts mitochondrial and endoplasmic reticulum (ER) function. Hypoxia has been shown to alter mitochondrial reactive oxygen species (ROS) homeostasis and induce ER stress. Hypoxia during pregnancy is associated with excessive production of ROS in the placenta, leading to oxidative stress. Oxidative stress occurs in a number of human diseases, including high blood pressure during pregnancy. Studies have shown that uterine placental tissue/cells in preeclampsia and IUGR show high levels of oxidative stress, which plays an important role in the pathogenesis of both the complications. This review summarizes the role of hypoxia-induced mitochondrial oxidative stress and ER stress in the pathogenesis of preeclampsia/IUGR and discusses the potential therapeutic strategies targeting oxidative stress to treat both the pregnancy complications.
Pregnancy ; Female ; Humans ; Placenta ; Fetal Growth Retardation/etiology* ; Pre-Eclampsia/pathology* ; Reactive Oxygen Species ; Hypoxia/pathology* ; Pregnancy Complications/pathology* ; Endoplasmic Reticulum Stress

OBJECTIVE: To explore the effect of hypoxia-supported umbilical cord mesenchymal stem cell (UC-MSC) on the expansion of cord blood mononuclear cell （MNC） in vitro. METHODS: The isolated cord blood mononuclear cells were inoculated on the preestablished umbilical cord mesenchymal stem cell layer and cultured under hypoxic conditions (3％ O₂) and the experimental groups were normoxia (MNCs were cultured under normoxic conditions), hypoxia (MNCs were cultured under hypoxic conditions), UC-MSC (MNCs were cultured with UC-MSC under normoxic conditions), and UC-MSC+hypoxia (MNCs were cultured with UC-MSC under hypoxic conditions). To further investigate the combinational effect of 3 factors of SCF+FL+TPO (SFT) on expansion of cord blood MNCs in vitro in hypoxia-supported UC-MSC culture system, the experiments were further divided into group A (MNCs were cultured with UC-MSC and SFT under normoxic conditions), group B (MNCs were cultured with UC-MSC under hypoxic conditions), group C (MNCs were cultured with UC-MSC and SFT under hypoxic conditions). The number of nucleated cells (TNC), CD34⁺ cell, CFU and CD34⁺CXCR4⁺, CD34⁺CD49d⁺, CD34⁺CD62L⁺ cells of each groups were detected at 0, 7, 10 and 14 days, respectively. RESULTS: Compared with group hypoxia and UC-MSC, group UC-MSC+hypoxia effectively promoted the expansion of TNC, CD34⁺ cell and CFU, and upregulated the expression level of adhesion molecule and CxCR4 of the cord blood CD34⁺ cell（P<0.05）. After culturing for 14 days, compared with group A and group B, group C effectively promoted the expansion of cord blood MNC at different time points（P<0.05）, and the effect of group A was better than that of group B at 7 and 10 days（P<0.05）. CONCLUSION Hypoxia-supported UC-MSC efficiently promoted the expansion and expression of adhesion molecule and CXCR4 of cord blood CD34⁺ cell, and the effect of expansion could be enhanced when SFT 3 factors were added.
Humans ; Cells, Cultured ; Fetal Blood ; Cell Proliferation ; Umbilical Cord/metabolism* ; Mesenchymal Stem Cells ; Antigens, CD34/metabolism* ; Hypoxia/metabolism*

BACKGROUND: Beyond its current function as a rescue therapy in acute respiratory distress syndrome (ARDS), extracorporeal membrane oxygenation (ECMO) may be applied in ARDS patients with less severe hypoxemia to facilitate lung protective ventilation. The purpose of this study was to evaluate the efficacy of extended ECMO use in ARDS patients. METHODS: This study reviewed 223 adult patients who had been admitted to the intensive care units of 11 hospitals in Korea and subsequently treated using ECMO. Among them, the 62 who required ECMO for ARDS were analyzed. The patients were divided into two groups according to pre-ECMO arterial blood gas: an extended group (n=14) and a conventional group (n=48). RESULTS: Baseline characteristics were not different between the groups. The median arterial carbon dioxide tension/fraction of inspired oxygen (FiO2) ratio was higher (97 vs. 61, p<0.001) while the median FiO2 was lower (0.8 vs. 1.0, p<0.001) in the extended compared to the conventional group. The 60-day mortality was 21% in the extended group and 54% in the conventional group (p=0.03). Multivariate analysis indicated that the extended use of ECMO was independently associated with reduced 60-day mortality (odds ratio, 0.10; 95% confidence interval, 0.02–0.64; p=0.02). Lower median peak inspiratory pressure and median dynamic driving pressure were observed in the extended group 24 hours after ECMO support. CONCLUSION: Extended indications of ECMO implementation coupled with protective ventilator settings may improve the clinical outcome of patients with ARDS.
Adult ; Anoxia ; Carbon Dioxide ; Extracorporeal Membrane Oxygenation ; Humans ; Intensive Care Units ; Korea ; Lung ; Mortality ; Multicenter Studies as Topic ; Multivariate Analysis ; Oxygen ; Respiration, Artificial ; Respiratory Distress Syndrome, Adult ; Retrospective Studies ; Ventilation ; Ventilators, Mechanical

PURPOSE: The aim of this study was to investigate whether propofol could attenuate hypoxia/reoxygenation-induced apoptosis and autophagy in human renal proximal tubular cells (HK-2) by inhibiting JNK activation. MATERIALS AND METHODS: HK-2 cells were treated with or without propofol or JNK inhibitor SP600125 for 1 hour and then subjected to 15 hours of hypoxia and 2 hours of reoxygenation (H/R). Cell viability and LDH release were measured with commercial kits. Cell apoptosis was evaluated by flow cytometry. The expressions of p-JNK, cleaved-caspase-3, Bcl-2, and autophagy markers LC3 and p62 were measured by Western blot or immunofluorescence. RESULTS: HK-2 cells exposed to H/R insult showed higher cell injury (detected by increased LDH release and decreased cell viability), increased cell apoptosis index and expression of cleaved-caspase-3, a decrease in the expression of Bcl-2 accompanied by increased expression of p-JNK and LC3II, and a decrease in expression of p62. All of these alterations were attenuated by propofol treatment. Similar effects were provoked upon treatment with the JNK inhibitor SP600125. Moreover, the protective effects were more obvious with the combination of propofol and SP600125. CONCLUSION: These results suggest that propofol could attenuate hypoxia/reoxygenation induced apoptosis and autophagy in HK-2 cells, probably through inhibiting JNK activation.
Anoxia ; Apoptosis ; Autophagy ; Blotting, Western ; Cell Survival ; Flow Cytometry ; Fluorescent Antibody Technique ; Humans ; Propofol

PURPOSE: Hepatocellular carcinoma (HCC) is a common cancer worldwide. Metastasis-associated lung adenocarcinoma transcript 1 (MALAT1), a long noncoding RNA (lncRNA), has been reported to be aberrantly expressed in hypoxic cancer cells. MALAT1 plays a significant role in many malignancies, including HCC. The aim of this study was to explore the role of MALAT1 in hypoxic HCC cells and its underlying regulatory mechanism. MATERIALS AND METHODS: Quantitative reverse transcription PCR (qRT-PCR) assay was performed to detect the mRNA levels of MALAT1 and microRNA-200a (miR-200a) in HCC cells. Cell invasion and migration ability were evaluated by Transwell assay. Starbase v2.0 and luciferase reporter assay were employed to identify the association between MALAT1 and miR-200a. Cell proliferation and apoptosis were measured by MTT assay and flow cytometry, respectively. RESULTS: MALAT1 levels were significantly upregulated in HCC cells under hypoxia. Hypoxia promoted proliferation, migration, and invasion, and blocked apoptosis in Hep3B cells, which were weakened by knockdown of MALAT1. Starbase v2.0 showed that MALAT1 and miR-200a have a complementarity region, and luciferase reporter assay verified that MALAT1 interacted with miR-200a in Hep3B cells. Moreover, MALAT1 negatively regulated the expression of miR-200a. miR-200a levels were dramatically downregulated in HCC cells under hypoxia. Upregulation of miR-200a inhibited proliferation, migration, and invasion, and induced apoptosis in Hep3B cells under hypoxia. Interestingly, downregulation of miR-200a partially reversed the tumor-suppressive effect of knockdown of MALAT1 on Hep3B cells in hypoxic condition. CONCLUSION: LncRNA MALAT1 was involved in proliferation, migration, invasion, and apoptosis by interacting with miR-200a in hypoxic Hep3B cells, revealing a new mechanism of MALAT1 involved in hypoxic HCC progression.
Adenocarcinoma ; Anoxia ; Apoptosis ; Carcinoma, Hepatocellular ; Cell Proliferation ; Down-Regulation ; Flow Cytometry ; Luciferases ; Lung ; Polymerase Chain Reaction ; Reverse Transcription ; RNA, Long Noncoding ; RNA, Messenger ; Up-Regulation

BACKGROUND: Congenital central hypoventilation syndrome (CCHS) is a rare disorder characterized by alveolar hypoventilation and autonomic dysregulation. Patients with CCHS have adequate ventilation while awake but exhibit hypoventilation while asleep. More severely affected patients exhibit hypoventilation both when awake and when asleep. CASE: Here, we report a case of successful spinal anesthesia and postoperative epidural analgesia in a patient with CCHS who underwent orthostatic surgery. CONCLUSIONS: In patients with CCHS, anesthesia is used with the goal of minimizing respiratory depression to avoid prolonged mechanical ventilation. Regional anesthesia should be considered where appropriate. Continuous oxygen saturation and end-tidal carbon dioxide monitoring must be available.
Analgesia, Epidural ; Anesthesia ; Anesthesia, Conduction ; Anesthesia, Spinal ; Anoxia ; Carbon Dioxide ; Humans ; Hypoventilation ; Oxygen ; Respiration, Artificial ; Respiratory Insufficiency ; Ventilation

Whole body ultrasound can be used to improve the speed and accuracy of evaluation of an increasing number of organ systems in the critically ill. Cardiac and abdominal ultrasound can be used to identify the mechanisms and etiology of hemodynamic instability. In hypoxemia or hypercarbia, lung ultrasound can rapidly identify the etiology of the condition with an accuracy that is equivalent to that of computed tomography. For encephalopathy, ocular ultrasound and transcranial Doppler can identify elevated intracranial pressure and midline shift. Renal and bladder ultrasound can identify the mechanisms and etiology of renal failure. Ultrasound can also improve the accuracy and safety of percutaneous procedures and should be currently used routinely for central vein catheterization and percutaneous tracheostomy.
Anoxia ; Brain Diseases ; Catheterization ; Catheters ; Critical Care ; Critical Illness ; Hemodynamics ; Intensive Care Units ; Intracranial Hypertension ; Lung ; Operating Rooms ; Renal Insufficiency ; Tracheostomy ; Ultrasonography ; Urinary Bladder ; Veins

We present the case of a 48-year-old woman who complained of sustained dyspnea and newly developed dyspnea, who then suddenly and unexpectedly expired during bronchoscopy. On postmortem examination, the deceased had advanced gastric cancer as a primary tumor. Frequent lymphatic tumor emboli were observed with some pulmonary lymphangitic carcinomatosis (PLC), and pulmonary tumor thrombotic microangiopathy (PTMA). PLC and PTMA are lethal forms of pulmonary metastasis, and PTMA can lead to sudden death. The characteristic findings of PLC and PTMA in the deceased were not predominant, however, and the clinical manifestation was not acutely deteriorating. These findings are, therefore, insufficient to explain the deceased's sudden death. Clinically, the deceased manifested hypoxemia, bradycardia and cardiac arrest during bronchoscopy and then soon expired, suggesting the possibility of cardiovascular complication related to bronchoscopy. Despite several limitations, we assumed that the sudden unexpected death might have been induced by cardiovascular complications related to bronchoscopy and due to the underlying pathologic condition by PLC and PTMA.
Anoxia ; Autopsy ; Bradycardia ; Bronchoscopy ; Carcinoma ; Death, Sudden ; Dyspnea ; Female ; Forensic Pathology ; Heart Arrest ; Humans ; Middle Aged ; Neoplasm Metastasis ; Stomach Neoplasms ; Thrombotic Microangiopathies

Hypoxia inducible factor (HIF)-stabilizers are being developed for the renal anemia treatment. This small molecules inhibit prolyl hydroxylase domain (PHD)-containing enzymes, causing HIF activation instead of degradation under the state of normoxia, finally increase production of intrinsic erythropoiesis. Current treatment guidelines suggest that renal anemia should be treated mainly with iron and erythropoiesis stimulating agents (ESAs). But there are several complications and concerns such as hypertension, ESA refractory anemia and increased cardiovascular mortality in using ESAs. Advantages of HIF stabilizers over ESAs are orally available, no dose-up requirement for inflammation. So far new HIF stabilizers showed efficacy and safety in renal anemia treatment. This new therapeutic agent may emerge as a standard treatment option for renal anmia treatment.
Anemia ; Anemia, Refractory ; Anoxia ; Erythropoiesis ; Hematinics ; Hepcidins ; Humans ; Hypertension ; Inflammation ; Iron ; Mortality ; Prolyl Hydroxylases ; Renal Insufficiency, Chronic